Kharakov
Quantum Hot Dog
Dog shit is digested "food". God shit is digested "mind". I see it all over the place.Why is it that Gnu lovers always seem to believe in dog?
I believe that the dog kind exists due to evidence, not "belief in."
Dog shit is digested "food". God shit is digested "mind". I see it all over the place.Why is it that Gnu lovers always seem to believe in dog?
I believe that the dog kind exists due to evidence, not "belief in."
Here's the really simple version: you have a colony of bacteria. They are not all the same. Some are quite sensitive to an antibiotic, some are barely sensitive at all. When you take the first course of the antibiotic you change the environment to one that is toxic to the bacteria. All of the sensitive bacteria are no longer fit to survive in the environment and die. Many, but not all, of the insensitive bacteria die. Those that survive begin reproducing at a fairly standard bacterial rate of doubling every twenty minutes. Within a day or two they are back to their original numbers. The difference is that now there are no sensitive bacteria, only insensitive ones. As a result, next time you take the antibiotics, only a few bacteria die as they are now better adapted to the new environment. Now that they are comfortable, they enter a phase of genetic drift in which new variations spread out as mutations and Horizontal Gene Transfer increase the diversity of the population.
That's the quick version. Here's a long version:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982203/
Any questions?
I note you are still avoiding a proper response to my description of evolution. I'll post it again later for you as a helpful vade mecum and you can try again. Sadly, when I first left school I was fortunate to work for a few years at The unfortunately named National Institute for Research into Dairying where I specialised in the varying gut bacteria of milk cows. I've only got an HNC here, but I have three years of hands on experience dealing with gut bacteria, and to be fair, cowshit. It was only after I went to university that I changed gender.
The fact is that you are too good at avoiding the truth not to realise what the truth is. The way you worm around it shows that, however dimly, you know you are wrong. That leaves the question why you are doing it.
I still think it's religion and I just want to point out that the only reason religion hates evolution is that it answers the question, posed so many times by religion: there's so much good design in the world, how could it have got there without a designer. The fact is that evolution explains neatly just how that design got there without a deity. The stupid thing is that this isn't an argument about God, it's an argument against one argument for God. The faithful should just let it go and use other arguments, rather than making fools of themselves trying to fight a fight they are doomed to lose against people who understand the beauty and power of this explanation.
1.1. Genetic mutation
Darwin’s theory of evolution is perfectly epitomized by the progression of drug resistance in M. tuberculosis. Like any new traits arising during selective evolution, antibiotic resistant strains only become predominant in M. tuberculosis populations if the resistance phenotypes provide the mutants with survival advantages over their susceptible counterparts. The prolonged drug exposure due to lengthy regimens might have greatly contributed to the continued progression of the selective evolution of resistant strains that otherwise would hardly predominate the population because of their reduced fitness compared to susceptible strains.
Yet, the disease came back in the 1980s with outbreaks of multidrug resistant strains, often associated with the spreading epidemic of the acquired immune deficiency syndrome (AIDS).
all currently known acquired resistances are mediated through chromosomal mutations that arise under selective pressure of antibiotic use.
By definition, a chromosomal mutation is any change or error that occurs within the chromosome. Such errors can be attributed to any mistakes or problems that occur during cell processes like mitosis and meiosis.
Unlike gene mutations that involve the alteration of a gene or a segment of DNA in the chromosome, chromosomal mutations occur and change the entirety of the chromosome itself.
Three types of chromosomal mutations exist: mutations on the structure of chromosomes, mutations on the chromosome number, and mutations on the sex chromosomes.
Possible interconnections of the TCA cycle, cellular redox homeostasis and action of bactericidal antibiotics in M. tuberculosis. The primary interactions between bactericidal antibiotics and their targets trigger oxidation of NADH, produced in the TCA cycle, through the electron transport chain. This leads to increased production of superoxide that destroys iron-sulfur clusters yielding iron for oxidation of the Fenton reaction. The Fenton reaction results in the formation of hydroxyl radicals that damage nucleic acids, proteins, and lipid, eventually leading to cell death. However, if a cell survives, these hydroxyl radicals increase its mutagenesis thus promoting the emergence of MDR strains. The current TB drugs isoniazid (INH) and ethionamide (ETH) kill mycobacteria via direct conversion to free radicals that may contribute to the formation of MDR M. tuberculosis strains. The recently discovered MDR determinant PknG might regulate activity of many enzymes of the TCA cycle via its phosphorylation of GarA. These enzymes (KGD, GS, and GDH, in red) might affect the cellular NADH pool required for the downstream electron transport chain triggered by bactericidal antibiotics thus leading to cell death. MD: malate dehydrogenase, ICD: isocitrate dehydrogenase. Redrawn with modifications from (Kohanski et al. 2007).
TL;DRYou better demand your money back because the education you received were fraud after fraud those guys put inside your brain.
First at all, the dude who wrote the essay or article is clearly a fanatic of evolution, you can tell because he enforces the doctrines of the theory instead of giving the analysis based on the observation without giving personal beliefs.
Second, the scenario he has presented is not the general scenario.
You and possibly him are assuming that the whole bacteria which were sensitive to the antibiotics died and the ones which weren't sensitive survived and populated back very fast and replaced the ones which were gone.
If that is true, then nobody should recover from bacteria attacks using antibiotics. If that is his point and yours, then no antibiotics should work at all!
Such idea is peanuts.
Get it?
Lets see what this dude preaches, have you bible at hand... this is to say, you Darwin book.
" provide the mutants with survival advantages over their susceptible counterparts." What a wonderful stupidity.
He first mixes the recent increasing of Tuberculosis thanks to the presence of AIDS.
Yet, the disease came back in the 1980s with outbreaks of multidrug resistant strains, often associated with the spreading epidemic of the acquired immune deficiency syndrome (AIDS).
Then, it is not tuberculosis bacteria alone but human body's decay or degeneration by causes of other infection. In this case a virus.
Are you with me?
Good.
Lets go to the AIDS virus.
There are people who have been catalogued as having a "natural resistance to the AIDS virus".
After a deep study, it was found out that it wasn't any "resistance". People who were exposed to the virus and acquired it but weren't affected, was because their immune cells were "DEFORMED". Lol.
Yup. The AIDS virus uses the "hair" of the human body immune cells like Tarzan swings through the jungle by hanging from a wine. People who were born with the defect of having their body immune system with "bold" cells, didn't provide the method of transportation for the AIDS viruses.
As you can see, there is no "evolution" and there is no "adaptation", no "speciation" nothing of what this dude of the link and you are trying to sell. And, be born with "bold" immune system cells is not "favorable" because only saves you from viruses like the AIDS virus, however it won't help you for resisting catching a cold.
And to be exposed to AIDS is not a "nature thing", so there is no reason for the human species to "speciate" against AIDS.
So, we have supposedly the dude mechanism:
all currently known acquired resistances are mediated through chromosomal mutations that arise under selective pressure of antibiotic use.
"Chromosomal mutations."
Lets see what are those.
https://www.bioexplorer.net/chromosomal-mutations.html/
By definition, a chromosomal mutation is any change or error that occurs within the chromosome. Such errors can be attributed to any mistakes or problems that occur during cell processes like mitosis and meiosis.
Unlike gene mutations that involve the alteration of a gene or a segment of DNA in the chromosome, chromosomal mutations occur and change the entirety of the chromosome itself.
Three types of chromosomal mutations exist: mutations on the structure of chromosomes, mutations on the chromosome number, and mutations on the sex chromosomes.
Errors, mistakes or problems happening in the process and with a chromosome.
Great!
You were born with Down Syndrome, then you have "evolved"! That error, mistake, problem in your chromosomes made you more "resistant" to better educated people.
See the situation here?
The Tuberculosis bacteria is not more resistant, it has suffered an UNFAVORABLE change, its chromosomes are now replicated with errors, mistakes and problems. Darwin was wrong. Period.
You are being witness here that this dude has imposed his scientific religious beliefs on Darwin's theory rather than analyzing, evaluating and having conclusions with impartial judgement. A true scientists won't promote a theory with the results of a tests or an observation. The most closer they go is saying, "it appears that such theory might be correct", or "this result might corroborate the hypothesis of..."
Only facts can be asserted without discussion, but theoretical stuff is always exposed to error, and only mediocre dudes or paid under the table scientists spread out propaganda in favor of a theory.
Lets go to the explanation of the mechanism of the process of antibiotics in bacteria (this is about M.Tuberculosis alone.)
Possible interconnections of the TCA cycle, cellular redox homeostasis and action of bactericidal antibiotics in M. tuberculosis. The primary interactions between bactericidal antibiotics and their targets trigger oxidation of NADH, produced in the TCA cycle, through the electron transport chain. This leads to increased production of superoxide that destroys iron-sulfur clusters yielding iron for oxidation of the Fenton reaction. The Fenton reaction results in the formation of hydroxyl radicals that damage nucleic acids, proteins, and lipid, eventually leading to cell death. However, if a cell survives, these hydroxyl radicals increase its mutagenesis thus promoting the emergence of MDR strains. The current TB drugs isoniazid (INH) and ethionamide (ETH) kill mycobacteria via direct conversion to free radicals that may contribute to the formation of MDR M. tuberculosis strains. The recently discovered MDR determinant PknG might regulate activity of many enzymes of the TCA cycle via its phosphorylation of GarA. These enzymes (KGD, GS, and GDH, in red) might affect the cellular NADH pool required for the downstream electron transport chain triggered by bactericidal antibiotics thus leading to cell death. MD: malate dehydrogenase, ICD: isocitrate dehydrogenase. Redrawn with modifications from (Kohanski et al. 2007).
Look, you can even see the diagram, how after the oxidation reaction will give as consequence the death of the cell or "increased mutation rates".
The drug is causing cellular proteolysis, which is known if not controlled will cause the degradation of proteins.
The survivors will carry chromosomes with degraded proteins, the consequence will be mutations for the next generation or replica.
Ask yourself the question.
How in the word a degraded bacteria will be "more resistant" to antibiotics?
The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
If you might be so kind to show the specifics.
The link only mention the wonderful "evolution of mutated bacteria" in front of antibiotics, but that's all. The diagram explain the process until bacteria or dies or mutates.
It is not explaining the new mutated bacteria.
Do you get the point?
Or die or mutate.
It mutated. Then, what happened?
Show me with this analogy.
The bacteria before antibiotics had 2 million hairs, a gigantic mouth, clutches, long legs, great vision, big teeth, etc.
After a treatment with antibiotics, what happened? Why mutated bacteria is not affected anymore?
Your link has explained why some bacteria survives and with some died, however, saying "mutations made them drug resistant" is not the total explanation.
I'm not asking the mechanism of proteolysis in M. Tuberculosis or cells in general, which until today is hard to be understood, but the mechanism of why bacteria is not affected by some drugs to which was exposed before, that one yes, it does have an explanation.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
Wiki said:Mechanism of action[edit]
Tetracycline antibiotics are protein synthesis inhibitors, inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex. They do so mainly by binding to the 30S ribosomal subunit in the mRNA translation complex.[17]
Tetracyclines also have been found to inhibit matrix metalloproteinases. This mechanism does not add to their antibiotic effects, but has led to extensive research on chemically modified tetracyclines or CMTs (like incyclinide) for the treatment of rosacea, acne, diabetes and various types of neoplasms.[18][19][20] Incyclinide was announced to be ineffective for rosacea in September 2007.[21]
Several trials have examined modified and unmodified tetracyclines for the treatment of human cancers; of those, very promising results were achieved with CMT-3 for patients with Kaposi Sarcoma.[22]
Wiki said:Mechanism of resistance[edit]
Tetracycline inhibits cell growth by inhibiting translation. It binds to the 16S part of the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature.
Cells become resistant to tetracycline by at least three mechanisms: enzymatic inactivation of tetracycline, efflux, and ribosomal protection. Inactivation is the rarest type of resistance, where an acetyl group is added to the molecule, causing inactivation of the drug. In efflux, a resistance gene encodes a membrane protein that actively pumps tetracycline out of the cell. This is the mechanism of action of the tetracycline resistance gene on the artificial plasmid pBR322. In ribosomal protection, a resistance gene encodes a protein that can have several effects, depending on what gene is transferred. Six classes of ribosomal protection genes/proteins have been found, all with high sequence homology, suggesting a common evolutionary ancestor.
Possible mechanisms of action of these protective proteins include:
blocking tetracyclines from binding to the ribosome
binding to the ribosome and distorting the structure to still allow t-RNA binding while tetracycline is bound
binding to the ribosome and dislodging tetracycline.
All of these changes to ribosomes are reversible (non-covalent) because ribosomes isolated from both tetracycline-resistant and susceptible organisms bind tetracycline equally well in vitro.
You better demand your money back because the education you received were fraud after fraud those guys put inside your brain.
First at all, the dude who wrote the essay or article is clearly a fanatic of evolution, you can tell because he enforces the doctrines of the theory instead of giving the analysis based on the observation without giving personal beliefs.
Second, the scenario he has presented is not the general scenario.
You and possibly him are assuming that the whole bacteria which were sensitive to the antibiotics died and the ones which weren't sensitive survived and populated back very fast and replaced the ones which were gone.
If that is true, then nobody should recover from bacteria attacks using antibiotics. If that is his point and yours, then no antibiotics should work at all!
Such idea is peanuts.
Get it?
Source said:" provide the mutants with survival advantages over their susceptible counterparts."
HM said:What a wonderful stupidity.
He first mixes the recent increasing of Tuberculosis thanks to the presence of AIDS.
source said:Yet, the disease came back in the 1980s with outbreaks of multidrug resistant strains, often associated with the spreading epidemic of the acquired immune deficiency syndrome (AIDS).
Then, it is not tuberculosis bacteria alone but human body's decay or degeneration by causes of other infection. In this case a virus.
Are you with me?
Good.
Lets go to the AIDS virus.
There are people who have been catalogued as having a "natural resistance to the AIDS virus".
HM said:
After a deep study, it was found out that it wasn't any "resistance". People who were exposed to the virus and acquired it but weren't affected, was because their immune cells were "DEFORMED". Lol.
Yup. The AIDS virus uses the "hair" of the human body immune cells like Tarzan swings through the jungle by hanging from a wine. People who were born with the defect of having their body immune system with "bold" cells, didn't provide the method of transportation for the AIDS viruses.
And, be born with "bold" immune system cells is not "favorable" because only saves you from viruses like the AIDS virus, however it won't help you for resisting catching a cold.
HM said:And to be exposed to AIDS is not a "nature thing", so there is no reason for the human species to "speciate" against AIDS.
So, we have supposedly the dude mechanism:
HM said:all currently known acquired resistances are mediated through chromosomal mutations that arise under selective pressure of antibiotic use.
"Chromosomal mutations."
Lets see what are those.
https://www.bioexplorer.net/chromosomal-mutations.html/
By definition, a chromosomal mutation is any change or error that occurs within the chromosome. Such errors can be attributed to any mistakes or problems that occur during cell processes like mitosis and meiosis.
Unlike gene mutations that involve the alteration of a gene or a segment of DNA in the chromosome, chromosomal mutations occur and change the entirety of the chromosome itself.
Three types of chromosomal mutations exist: mutations on the structure of chromosomes, mutations on the chromosome number, and mutations on the sex chromosomes.
Errors, mistakes or problems happening in the process and with a chromosome.
Great!
You were born with Down Syndrome, then you have "evolved"! That error, mistake, problem in your chromosomes made you more "resistant" to better educated people.
See the situation here?
The Tuberculosis bacteria is not more resistant, it has suffered an UNFAVORABLE change, its chromosomes are now replicated with errors, mistakes and problems.
Darwin was wrong. Period.
You are being witness here that this dude has imposed his scientific religious beliefs on Darwin's theory rather than analyzing, evaluating and having conclusions with impartial judgement.
A true scientists won't promote a theory with the results of a tests or an observation.
Evidence thus far indicates that pathogenic bacteria such as M. tuberculosis are well able to cope with this pressure and that they have evolved to become progressively resistant to antibiotics
HM said:The most closer they go is saying, "it appears that such theory might be correct", or "this result might corroborate the hypothesis of..."
scientists said:recent studies indicate
Evidence thus far indicates
This strategy might help
TB said:Only facts can be asserted without discussion, but theoretical stuff is always exposed to error, and only mediocre dudes or paid under the table scientists spread out propaganda in favor of a theory.
Lets go to the explanation of the mechanism of the process of antibiotics in bacteria (this is about M.Tuberculosis alone.
Science said:Possible interconnections of the TCA cycle, cellular redox homeostasis and action of bactericidal antibiotics in M. tuberculosis. The primary interactions between bactericidal antibiotics and their targets trigger oxidation of NADH, produced in the TCA cycle, through the electron transport chain. This leads to increased production of superoxide that destroys iron-sulfur clusters yielding iron for oxidation of the Fenton reaction. The Fenton reaction results in the formation of hydroxyl radicals that damage nucleic acids, proteins, and lipid, eventually leading to cell death. However, if a cell survives, these hydroxyl radicals increase its mutagenesis thus promoting the emergence of MDR strains. The current TB drugs isoniazid (INH) and ethionamide (ETH) kill mycobacteria via direct conversion to free radicals that may contribute to the formation of MDR M. tuberculosis strains. The recently discovered MDR determinant PknG might regulate activity of many enzymes of the TCA cycle via its phosphorylation of GarA. These enzymes (KGD, GS, and GDH, in red) might affect the cellular NADH pool required for the downstream electron transport chain triggered by bactericidal antibiotics thus leading to cell death. MD: malate dehydrogenase, ICD: isocitrate dehydrogenase. Redrawn with modifications from (Kohanski et al. 2007).
Look, you can even see the diagram, how after the oxidation reaction will give as consequence the death of the cell or "increased mutation rates".
The drug is causing cellular proteolysis, which is known if not controlled will cause the degradation of proteins.
The survivors will carry chromosomes with degraded proteins, the consequence will be mutations for the next generation or replica.
Ask yourself the question.
How in the word a degraded bacteria will be "more resistant" to antibiotics?
The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
The link only mention the wonderful "evolution of mutated bacteria" in front of antibiotics, but that's all. The diagram explain the process until bacteria or dies or mutates.
It is not explaining the new mutated bacteria.
Do you get the point?
Or die or mutate.
It mutated. Then, what happened?
Show me with this analogy.
The bacteria before antibiotics had 2 million hairs, a gigantic mouth, clutches, long legs, great vision, big teeth, etc.
After a treatment with antibiotics, what happened? Why mutated bacteria is not affected anymore?
Your link has explained why some bacteria survives and with some died, however, saying "mutations made them drug resistant" is not the total explanation.
I'm not asking the mechanism of proteolysis in M. Tuberculosis or cells in general, which until today is hard to be understood,
but the mechanism of why bacteria is not affected by some drugs to which was exposed before, that one yes, it does have an explanation.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
TL;DR
Almost all of the time there are no resistant bacteria. I recall the early antibiotics worked for years. During that time antibiotics were prescribed when they didn't know whether a virus or bacterial illness. And then, somewhere, after billions upon billions were killed by that antibiotic there was a mutation that made an individual resistant. Exponential growth occurred. The patient was given a different antibiotic and all was well. After billions of billions more it happened again. And again and again. Finally one survived. And grew enough to spread to another host. We now have a population resistant to two antibiotics. After more and more years one bacterium mutated to be resistant to 3. On and on to MRSA and others.
"Our results provide strong evidence that antibiotics change the baby's inherited microbial communities with long-term disease consequences, which is especially important given the widespread use of antibiotics in young women before and during pregnancy," says Martin Blaser, MD, the Muriel G. and George W. Singer Professor of Translational Medicine at NYU Langone Health, and the study's senior author.
"Our study shows that the changes made to the microbiome by antibiotic exposure can be transmitted across generations, from moms to their offspring, which is consistent with our work and that of others in humans," adds Blaser, also a professor of microbiology at NYU Langone.
Human intestinal bacteria have many roles in human health, most of which are beneficial or neutral for the host. In this review, we explore a more sinister side of intestinal bacteria; their role as traffickers in antibiotic resistance genes. Evidence is accumulating to support the hypothesis that intestinal bacteria not only exchange resistance genes among themselves but might also interact with bacteria that are passing through the colon, causing these bacteria to acquire and transmit antibiotic resistance genes.
Antibiotics save lives, but they are not fail-safe. Even when microbes haven’t acquired drug-evading genetic mutations—a hallmark of antibiotic resistance—the medications don’t always clear infections. A new study identifies a surprising reason why: At infection sites, antibiotics change the natural mixture of chemicals made by the body in ways that protect infecting bacteria. They also thwart the ability of the host’s immune cells to fight off the intruders.
These findings, published Thursday in Cell Host & Microbe, could help scientists “build more effective treatments,” says James Collins, a biological engineer at Massachusetts Institute of Technology and senior author of the paper. Down the line it may be possible to administer antibiotics along with other substances that either mitigate these changes or have the opposite effect, making drugs more effective, he says.
Ask yourself the question.
How in the word a degraded bacteria will be "more resistant" to antibiotics?
You are confusing yourself with your determined use of the word 'degraded' There simply isn't any way you can use the word sensibly here. The only word you can use is 'different'. Most different bacteria will be less well suited to the environment, but a few will be better adapted, just like the people with the CCR5 difference. These will survive to breed again, thus preserving and accumulating the improved fit to this particular environment. Even if you could use that word, it's the proteins and so on that are damaged, not the bacteria, the degraded proteins may confer an advantage, as we saw with HIV - the removasl of the CCR5 while damage, stops the HIV from getting into the cell...
The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
Yes, of the billions of bacteria and the many millions that are mutated, the overwhelming majority will simply die as the mutation renders them unfit. However, a diminishing minority will mutate in a way that is advantageous.
Sure, they go into detail in the very next paragraph, perhaps you should have read on. (although your ability to cherry pick is remarkable...)
In a search for M. tuberculosis proteins that bind the active molecule pyrazinoic acid, the 30S ribosomal protein S1 (RpsA) was identified (Shi et al. 2011). Over-expression of rspA results in increased pyrazinamide resistance (Shi et al. 2011). Sequencing of a non-pncA pyrazinamide resistant strain revealed a 3-base pair in-frame deletion that leads to loss of Alanine 438 at the C terminus of RspA (Shi et al. 2011). These observations suggested that RspA is involved in M. tuberculosis pyrazinamide resistance.
That mutation either left it better fitted for the environment or it didn't. If it didn't it would tend to die, if it did it would tend to survive. if it died, the unhelpful (in that environment) mutation is lost, if it survived then that helpful (in that environment) mutation would be preserved and contribute to the general fitness (in that environment) of its offspring that carried that mutation. That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
Show me with this analogy.
The bacteria is a guy, 6 feet tall, 180 lbs. regular dude, healthy, good IQ, hard worker man, etc. He will be under attack with chemicals. The mission is to kill him.
Use the method you want, could be dropping chemicals over him from a helicopter, giving him the chemicals in his food, you are free to choose the way to kill the guy in the example.
Show later, after the first attack, he will be attacked again with the same chemicals, but at this time he won't be affected, of if he does, will be very minimum.
Isn't it? it is clearly explained in that article: reactive oxygen and free radicals denature the protein, lipids and nucleic acid. That's a very clear and well understood process.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
It's a theory that comfortably explains everything above and one that I think you dimly grasp because you couldn't cherry pick as effectively if you didn't. Why are you so scared of evolution that you will deny the evidence in front of you? If it's not religion (but I still think it is) then why are you so against this theory in particular?
We passed that part -with the link provided-, showing what chromosomes mutations are about.
When you degrade proteins to combat HIV, you are also degrading protein for survival of the individual as a living organism.
Then, the solution for one thing is a new problem for the individual. You remind me an uncle whom for breakfast used to have about 7 pills of different sizes and colors. He used to smoke a lot and have some issues with blood flowing to his brain. He explained me, one was for making blood thinner so can pass thru almost blocked veins, but the pill causes stomach irritation, so he take a second pill for the stomach, but it causes heavy drowsiness, so he take the another pill for drowsing but it causes.... a chain of side effects and temporary remedies... for what? He died of lung cancer.
When you degrade the normal level of proteins in a person, you are causing harm... but you will save him from AIDS and mutants.
HM said:The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
Sub said:Yes, of the billions of bacteria and the many millions that are mutated, the overwhelming majority will simply die as the mutation renders them unfit. However, a diminishing minority will mutate in a way that is advantageous.
Now you are finally getting the point. The mutations are not favorable, because it will cause degenerate out comings in the species.
Now well, the new degenerate status, in the case of the bacterium in question, by chance and not by theoretical doctrines, is sometimes advantageous.
This situation is not backing up evolution. As I pointed before in another message in this topic, survival of the species and their changes are just being at the right place at the right moment. Thousands of years ago horses in Europe and Asia survived, but in America died and got extincted. Ones where in the right place and the right moment, the other ones didn't.
Simple.
HM said:If you might be so kind to show the specifics.[/B]
Sure, they go into detail in the very next paragraph, perhaps you should have read on. (although your ability to cherry pick is remarkable...)
In a search for M. tuberculosis proteins that bind the active molecule pyrazinoic acid, the 30S ribosomal protein S1 (RpsA) was identified (Shi et al. 2011). Over-expression of rspA results in increased pyrazinamide resistance (Shi et al. 2011). Sequencing of a non-pncA pyrazinamide resistant strain revealed a 3-base pair in-frame deletion that leads to loss of Alanine 438 at the C terminus of RspA (Shi et al. 2011). These observations suggested that RspA is involved in M. tuberculosis pyrazinamide resistance.
The test, what radiometric system was used? The BACTEC 37 460TB with BACTEC 460TB PZA?
Was the ACTEC MGIT 960 (BT960) 41 platform for PZA susceptibility?
I must encourage you to review that either test is not infallible and comparing both the discordance is notorious, not slight but very notorious.
Your link, by the origin of the agency must have used 460TB which is discontinued, and even if they use BT960, results can't be taken as accurate as well. It is needed a third method of test other than 460TB to verify BT960. (460TB is currently out of production).
In the "mechanism" shown above, the method of measure pyrazinamide susceptibility can be taken as an testimony but not as evidence because was not in agreement with the another method of measurement.
You have here a crucial challenge for the given results.
BACTEC 460 TB system which has been the "Gold Standard" for automated detection of TB.
Lets continue.
"Over-expression of rspa"
rspa a glycoprotein which in this case discussing here has the duty of binding to the 30S ribosomal protein S1.
What the mutation does is to "impair" the binding. This is to say, the binding is not strong anymore, it can get loose easily.
Like if you have your teeth binding strongly to your gums, the mutation will cause for you weak setting of the teeth in your mouth. They can fell out after eating an apple.
Is it "favorable" for bacteria having weak bonding in its structure?
What the hell is that "over-expression?"
Simply, the increased frequency of losing the characteristic of bonding.
HM said:"loss of Alanine"
Another degeneration like the horse losing functional digits. Another example for this case is, you lose your skin capabilities to protect you from the environment.
That is not "adaptation", that is not evolution", that is not "speciation", losing alenanine (amino acids) is degeneration.
Up to here, losing capabilities and structural damage and bonding is what antibiotics cause in our poor Tuberculosis bacterium.
Even so, for the next treatment using the same antibiotics, our hero, the Toobee bacterium survives it.
Wow!
You called it "resistant", the whole evolutionists called it "resistant".
However, for our Toobee bacterium, having a deformed body won't make it "resistant" to a new attack.
Think.
Think, because your link is not giving the answer.
Sub said:That mutation either left it better fitted for the environment or it didn't. If it didn't it would tend to die, if it did it would tend to survive. if it died, the unhelpful (in that environment) mutation is lost, if it survived then that helpful (in that environment) mutation would be preserved and contribute to the general fitness (in that environment) of its offspring that carried that mutation. That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
HM said:But, the bacteria have lost characteristics, there is no "accumulation" but lost of characteristics.
Show me the "accumulations".
=EBI have reviewed above each one of the points given in the assumed explanation of the mechanism, and the only thing you can read is the something similar to the following:
The huge truck hit on the small car caused the car's front lights smashed, the front ball joints went loose, the alignment disturbed and siding to the left, air condition condenser gone, radiator destroyed, engine pushed inside and under the car bumper falling out, and broken windshield on the passenger side due to passenger didn't use seat belt.
HM said:You are telling me that with these conditions, the car is now more "resistant" for the next hit by truck, who's driver is obfuscated to hit again in order to kill the driver of the car because he is his wife's love affair.
Where are the "accumulation of favorable steps"?
You are an evolutionist and now it happens that you yourself don't understand what he said.
Read again your phrase.
That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
"Positive"? HIV positive is something "favorable"... sure... right...
Here is your test of fire. This is an analogy.
Respond to the analogy applying the discussion topic, replacing the Tuberculosis bacterium by a dude.
If you can't explain it, it is possible because you can't understand evolution and less what I am explaining you several times by now.
Just get on with it.
Show me with this analogy.
The bacteria is a guy, 6 feet tall, 180 lbs. regular dude, healthy, good IQ, hard worker man, etc. He will be under attack with chemicals. The mission is to kill him.
Use the method you want, could be dropping chemicals over him from a helicopter, giving him the chemicals in his food, you are free to choose the way to kill the guy in the example.
Show later, after the first attack, he will be attacked again with the same chemicals, but at this time he won't be affected, of if he does, will be very minimum.
Sub said:Isn't it? it is clearly explained in that article: reactive oxygen and free radicals denature the protein, lipids and nucleic acid. That's a very clear and well understood process.
Apparently you never read the small print words at the bottom of documents, in this case the superfluous conclusion from the consequences of antibiotics in bacteria. Saying "more resistant" is not what is going on.
Read my example of people with bold immune cells, they are not "resistant" but simply "no affected" by the AIDS virus, solely because their defect. They catch a cold, they can suffer liver diseases, stomach problem because other bacteria and viruses won't use immune cells hair as their way to move easily inside the body. Is it a weird case. It is not any "evolutionary step" but a birth defect.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
It's a theory that comfortably explains everything above and one that I think you dimly grasp because you couldn't cherry pick as effectively if you didn't. Why are you so scared of evolution that you will deny the evidence in front of you? If it's not religion (but I still think it is) then why are you so against this theory in particular?
HM said:Because evolution is a scientific religion.
Don't forget to answer the analogy.
Answering properly the analogy from above is the best way to check how well you understand evolution. It is just changing the bacterium for a dude. From here, introduce a treatment with drugs to kill the dude. Show the effects. show that when the dude survives will be "more resistant" to the next attack.
Best wishes.
I don't think that link did what you think it did.
You'll need to be more precise: do you mean attacking HIV with antibiotics? or do you mean the simple fact that some people lack the CCR5 pathway? I'll say it again, you can't use words that express a value judgement without specifying a designer, a design the preferences of a community or, at the very least the environment the subject is in. In an environment with HIV lacking the CCR5 pathway is a massive improvement as it renders you immune to HIV and means you will survive to have children and tend to pass on your immunity. Those with CCR5 will tend to die.
Then, the solution for one thing is a new problem for the individual. You remind me an uncle whom for breakfast used to have about 7 pills of different sizes and colors. He used to smoke a lot and have some issues with blood flowing to his brain. He explained me, one was for making blood thinner so can pass thru almost blocked veins, but the pill causes stomach irritation, so he take a second pill for the stomach, but it causes heavy drowsiness, so he take the another pill for drowsing but it causes.... a chain of side effects and temporary remedies... for what? He died of lung cancer.
Yeah and you remind me of a Flat Earther. He commited suicide after his wife left him. And the moral of the story? Like you, I think he knew he was wrong and just couldn't admit it. Very sad.
When you degrade the normal level of proteins in a person, you are causing harm... but you will save him from AIDS and mutants.
I'm happy with that, the loss of CCR5 would under normal circumstances be a bad thing, however in the face of HIV it suddenly becomes a good thing. That's the importance of diversity - lots of different shuffles of the genetic deck so that when adversity comes some will be better adapted than others - these survive.
That's the key thing, you are picking out a single example of diversity and calling it degradation - however everything is different and there are no grounds for calling it better or worse.
HM said:The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
Sub said:Yes, of the billions of bacteria and the many millions that are mutated, the overwhelming majority will simply die as the mutation renders them unfit. However, a diminishing minority will mutate in a way that is advantageous.
Now you are finally getting the point. The mutations are not favorable, because it will cause degenerate out comings in the species.
Nope, read the bit in bold again: it's this minority that tend to survive and breed - the majority will tend to die rather rapidly.
Now well, the new degenerate status, in the case of the bacterium in question, by chance and not by theoretical doctrines, is sometimes advantageous.
So why call it degenerate when it is advantageous - more to the point this advantage will help it survive in the environment, fixing the change.
This situation is not backing up evolution. As I pointed before in another message in this topic, survival of the species and their changes are just being at the right place at the right moment. Thousands of years ago horses in Europe and Asia survived, but in America died and got extincted. Ones where in the right place and the right moment, the other ones didn't.
Simple.
Yup, there's diversity, those that are more fit for the environment tend to survive and breed. Easy. During the Pleistocene, things got really cold - horses migrated across the Bering straits land bridge and headed to warmer climes. Any that stayed in North America found the conditions to extreme too quickly and died. As the conditions warmed, the horses that migrated couldn't migrate back as there was no land bridge.
I just want to point out that the ED overgeneralization error is a classic sign of either being four or using words you are not familiar with. 'Extincted', sums up things up nicely.
HM said:If you might be so kind to show the specifics.[/B]
Sure, they go into detail in the very next paragraph, perhaps you should have read on. (although your ability to cherry pick is remarkable...)
In a search for M. tuberculosis proteins that bind the active molecule pyrazinoic acid, the 30S ribosomal protein S1 (RpsA) was identified (Shi et al. 2011). Over-expression of rspA results in increased pyrazinamide resistance (Shi et al. 2011). Sequencing of a non-pncA pyrazinamide resistant strain revealed a 3-base pair in-frame deletion that leads to loss of Alanine 438 at the C terminus of RspA (Shi et al. 2011). These observations suggested that RspA is involved in M. tuberculosis pyrazinamide resistance.
The test, what radiometric system was used? The BACTEC 37 460TB with BACTEC 460TB PZA?
Was the ACTEC MGIT 960 (BT960) 41 platform for PZA susceptibility?
I must encourage you to review that either test is not infallible and comparing both the discordance is notorious, not slight but very notorious.
Your link, by the origin of the agency must have used 460TB which is discontinued, and even if they use BT960, results can't be taken as accurate as well. It is needed a third method of test other than 460TB to verify BT960. (460TB is currently out of production).
In the "mechanism" shown above, the method of measure pyrazinamide susceptibility can be taken as an testimony but not as evidence because was not in agreement with the another method of measurement.
You have here a crucial challenge for the given results.
Wow, you have gone from ignoring it to making up a bullshit justification based on the test fro TB they used? Can you explain why they MUST have used 460 TB? And perhaps comment on this paper:
https://www.ncbi.nlm.nih.gov/pubmed/16329561
and explain what the words:
BACTEC 460 TB system which has been the "Gold Standard" for automated detection of TB.
Mean? Look, you are not a scientist and so when you try to spout bullshit like this you just look bloody stupid. More to the point, you still haven't responded to the original point, merely tried to undermine it. Unsuccessfully.
Lets continue.
I can barely contain myself.
"Over-expression of rspa"
rspa a glycoprotein which in this case discussing here has the duty of binding to the 30S ribosomal protein S1.
What the mutation does is to "impair" the binding. This is to say, the binding is not strong anymore, it can get loose easily.
Like if you have your teeth binding strongly to your gums, the mutation will cause for you weak setting of the teeth in your mouth. They can fell out after eating an apple.
You do realise just how silly this conflation of a chemical term and a folk term looks. No, of course you don't. Here's one example: what would happen if the binding of oxygen in haemoglobin was strong? you'd asphyxiate as the oxygen would never get released. Whether a strong or weak binding is positive or negative is relative to what it's doing - it's not a degradation, it's just different.
Is it "favorable" for bacteria having weak bonding in its structure?
That depends entirely on the environment and what the bonding is doing.
What the hell is that "over-expression?"
Simply, the increased frequency of losing the characteristic of bonding.
Nope.
HM said:"loss of Alanine"
Another degeneration like the horse losing functional digits. Another example for this case is, you lose your skin capabilities to protect you from the environment.
Again, it's just different. In both cases it depends on the environment. With the fused foot, horses can run faster for longer. That was clearly and advantage at some point. Probably when it met some fast predators.
That is not "adaptation", that is not evolution", that is not "speciation", losing alenanine (amino acids) is degeneration.
It really isn't, it's just different. Perhaps you want to explore this in context rather than grabbing three words and obsessing about the word loss.
Up to here, losing capabilities and structural damage and bonding is what antibiotics cause in our poor Tuberculosis bacterium.
Even so, for the next treatment using the same antibiotics, our hero, the Toobee bacterium survives it.
Wow!
And again, you somehow know to completely ignore my careful explanation of what is going on. That's the smoking gun. the thing you can't bear to engage with. You do, dimly realise the problem with your account, because natural selection is so simple even someone with no education in the area and in terrible denial can see the truth of it, so you ignore it over and over again, while holding on to the simplistic idea that loss of anything means degeneration. You must really struggle with the degeneration of people losing weight, or the degeneration of having a cancer removed and so on.
YOu are giving away your awareness of the problem by ignoring the same ideas over and over again - and indeed ignoring me pointing this out over and over again.
You called it "resistant", the whole evolutionists called it "resistant".
That's right.
However, for our Toobee bacterium, having a deformed body won't make it "resistant" to a new attack.
Think.
Think, because your link is not giving the answer.
Yes it is, very simply. Just like the people without the CCR5, the lack of something stops the infection or the poisoning from doing its damage. As a result, the person or bacteria survives and survives to breed, passing on this variation to the next generation.
Sub said:That mutation either left it better fitted for the environment or it didn't. If it didn't it would tend to die, if it did it would tend to survive. if it died, the unhelpful (in that environment) mutation is lost, if it survived then that helpful (in that environment) mutation would be preserved and contribute to the general fitness (in that environment) of its offspring that carried that mutation. That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
HM said:But, the bacteria have lost characteristics, there is no "accumulation" but lost of characteristics.
The lack of, for example, CCR5, is a characteristic. It's one among many millions. All of the time, reproduction, mutation, transcription errors and so on increase the variation, the number of different characteristics - that's a load of processes increasing the number of characteristics all the time. Meanwhile natural selection eliminates the least successful and accumulates the most successful as those with these characteristics survive to breed.
Show me the "accumulations".
I just did. You'll ignore it, again, becuae you dimly see where youa re wrong but can't bring yourself to admit it.
=EBI have reviewed above each one of the points given in the assumed explanation of the mechanism, and the only thing you can read is the something similar to the following:
Really? you can't have been paying much attention then.
The huge truck hit on the small car caused the car's front lights smashed, the front ball joints went loose, the alignment disturbed and siding to the left, air condition condenser gone, radiator destroyed, engine pushed inside and under the car bumper falling out, and broken windshield on the passenger side due to passenger didn't use seat belt.
Bu that's nothing like what I described. What I described is a massive community of people driving cars. Each one customises their car so every car is lightly different. Some, for example, fit wet weather tyres, some fit jacked up suspension and some strip out the extra weight to improve acceleration.
Then depending on the environment each of these variations confers different advantages. If the area has flooding then the jacked up suspension will allow some cars to drive through puddles while the others get flooded and are scrapped. If racing becomes popular, then the stripped down cars will do better and the jacked up cars will be scrapped. All the time people are trying new customisations and the conditions are always changing. As a result, there will be a tendency for the succesful variations to carry on, buit these too will be modified so there is always more variation to be tested.
That's what I was saying.
HM said:You are telling me that with these conditions, the car is now more "resistant" for the next hit by truck, who's driver is obfuscated to hit again in order to kill the driver of the car because he is his wife's love affair.
Where are the "accumulation of favorable steps"?
No, I'm telling you that once again this is a silly straw man that doesn't remotely represent what I said. Again.
You are an evolutionist and now it happens that you yourself don't understand what he said.
So you keep saying.
Read again your phrase.
That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
"Positive"? HIV positive is something "favorable"... sure... right...
And again, you are deliberately equivocating on the word positive. This is simplyu dishonest and inexcusable. The word positive in HIV positive just means that you have HIV, Positive in the sense of mutation just means that the mutation helps you survive in a particular environment.
____________________________________________________________________
Here is your test of fire. This is an analogy.
Why should I bother, you literally ignored my response to the last challenge. I wonder why that was. Well I don't I think it's because you know you are wrong but think if you keep pushing you'll somehow justify yourself. You will not.
Respond to the analogy applying the discussion topic, replacing the Tuberculosis bacterium by a dude.
If you can't explain it, it is possible because you can't understand evolution and less what I am explaining you several times by now.
Just get on with it.Show me with this analogy.
The bacteria is a guy, 6 feet tall, 180 lbs. regular dude, healthy, good IQ, hard worker man, etc. He will be under attack with chemicals. The mission is to kill him.
Use the method you want, could be dropping chemicals over him from a helicopter, giving him the chemicals in his food, you are free to choose the way to kill the guy in the example.
Show later, after the first attack, he will be attacked again with the same chemicals, but at this time he won't be affected, of if he does, will be very minimum.
Hang on. You are talking about a single guy who dies? I'm sorry to break this to you, but after the first attack this single guy will be dead. The end. Your example is fatally flawed as it has only a single person
In the bacteria example, there will be billions of bacteria and only some will die. The survivors will survive to breed the rest will die.
So for a realistic example let's take a million people and expose them to HIV. one percent of these people don't have a CCR5. They tend to survive. The rest do and tend to die. As a result, in the next generation the majority of people will inherit a lack of a CCR5 pathway and will not become infected. That's so simple i know you must understand it. Which is why I suspect you'll ignore it.
Again.
Sub said:Isn't it? it is clearly explained in that article: reactive oxygen and free radicals denature the protein, lipids and nucleic acid. That's a very clear and well understood process.
Apparently you never read the small print words at the bottom of documents, in this case the superfluous conclusion from the consequences of antibiotics in bacteria. Saying "more resistant" is not what is going on.
Really. Can you give me the precise page number or cut and paste this 'fine print' because I think you just made it up. YOu are so desperate you are resorting to simply saying things that are not true. You can't be doing that by accident.
Read my example of people with bold immune cells, they are not "resistant" but simply "no affected" by the AIDS virus, solely because their defect. They catch a cold, they can suffer liver diseases, stomach problem because other bacteria and viruses won't use immune cells hair as their way to move easily inside the body. Is it a weird case. It is not any "evolutionary step" but a birth defect.
If you want to call something a defect when it stops you from getting HIV then you are going to have to explain the negative effects. What is the precise downside of not having a CCR5 pathway? The upside is clear you don't get HIV. The downsides you describe are simply fantasy. YOu made them up.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
It's a theory that comfortably explains everything above and one that I think you dimly grasp because you couldn't cherry pick as effectively if you didn't. Why are you so scared of evolution that you will deny the evidence in front of you? If it's not religion (but I still think it is) then why are you so against this theory in particular?
HM said:Because evolution is a scientific religion.
I explained why that made no sense las time. However, you know you are wrong. you wouldn't be able to cherrypick so effectively if you didn't grasp what undermines your account and your increasing reliance on fallacies and fantasies demonstrates your desperation.
Don't forget to answer the analogy.
I did, he died. the end.
Answering properly the analogy from above is the best way to check how well you understand evolution. It is just changing the bacterium for a dude. From here, introduce a treatment with drugs to kill the dude. Show the effects. show that when the dude survives will be "more resistant" to the next attack.
You are quite right. I can only assume that you mean me to work out who the dude is. Let me see, who is a the dude that some people think can die and then come back to life... Who could it be? dies and then comes back to life so you can perform the test a second time. It's Jesus isn't it. So Jesus, isn't killed because of whatever bollocks it is Christians believe about Jesus returning from the dead, presumably as a zombie. So this confers a selective advantage over other humans because he's indestructible. So when he fucks Mary Magdalene and produces a line of little Jesi, psion, I believe they are clled, is this a characteristic that can be passed on? I don't know, finally there's an area you can talk about with authority.
is eternal life transmissible genetically?
Now I've finished taking the piss out of your daft demonstration, I just have to point out that a single example doesn't introduce variation. A billion people? I've answered already.
Best wishes.
Thanks.
I don't think that link did what you think it did.
You'll need to be more precise: do you mean attacking HIV with antibiotics? or do you mean the simple fact that some people lack the CCR5 pathway? I'll say it again, you can't use words that express a value judgement without specifying a designer, a design the preferences of a community or, at the very least the environment the subject is in. In an environment with HIV lacking the CCR5 pathway is a massive improvement as it renders you immune to HIV and means you will survive to have children and tend to pass on your immunity. Those with CCR5 will tend to die.
Yeah and you remind me of a Flat Earther. He commited suicide after his wife left him. And the moral of the story? Like you, I think he knew he was wrong and just couldn't admit it. Very sad.
I'm happy with that, the loss of CCR5 would under normal circumstances be a bad thing, however in the face of HIV it suddenly becomes a good thing. That's the importance of diversity - lots of different shuffles of the genetic deck so that when adversity comes some will be better adapted than others - these survive.
That's the key thing, you are picking out a single example of diversity and calling it degradation - however everything is different and there are no grounds for calling it better or worse.
HM said:The assumed explanation in your link, as far as I have reviewed it, is not telling the mechanism of why the mutated bacteria is not affected anymore by antibiotics. It only says how it gets mutated by the cause of the drug.
Sub said:Yes, of the billions of bacteria and the many millions that are mutated, the overwhelming majority will simply die as the mutation renders them unfit. However, a diminishing minority will mutate in a way that is advantageous.
Now you are finally getting the point. The mutations are not favorable, because it will cause degenerate out comings in the species.
Nope, read the bit in bold again: it's this minority that tend to survive and breed - the majority will tend to die rather rapidly.
Now well, the new degenerate status, in the case of the bacterium in question, by chance and not by theoretical doctrines, is sometimes advantageous.
So why call it degenerate when it is advantageous - more to the point this advantage will help it survive in the environment, fixing the change.
This situation is not backing up evolution. As I pointed before in another message in this topic, survival of the species and their changes are just being at the right place at the right moment. Thousands of years ago horses in Europe and Asia survived, but in America died and got extincted. Ones where in the right place and the right moment, the other ones didn't.
Simple.
Yup, there's diversity, those that are more fit for the environment tend to survive and breed. Easy. During the Pleistocene, things got really cold - horses migrated across the Bering straits land bridge and headed to warmer climes. Any that stayed in North America found the conditions to extreme too quickly and died. As the conditions warmed, the horses that migrated couldn't migrate back as there was no land bridge.
I just want to point out that the ED overgeneralization error is a classic sign of either being four or using words you are not familiar with. 'Extincted', sums up things up nicely.
HM said:If you might be so kind to show the specifics.[/B]
Sure, they go into detail in the very next paragraph, perhaps you should have read on. (although your ability to cherry pick is remarkable...)
In a search for M. tuberculosis proteins that bind the active molecule pyrazinoic acid, the 30S ribosomal protein S1 (RpsA) was identified (Shi et al. 2011). Over-expression of rspA results in increased pyrazinamide resistance (Shi et al. 2011). Sequencing of a non-pncA pyrazinamide resistant strain revealed a 3-base pair in-frame deletion that leads to loss of Alanine 438 at the C terminus of RspA (Shi et al. 2011). These observations suggested that RspA is involved in M. tuberculosis pyrazinamide resistance.
The test, what radiometric system was used? The BACTEC 37 460TB with BACTEC 460TB PZA?
Was the ACTEC MGIT 960 (BT960) 41 platform for PZA susceptibility?
I must encourage you to review that either test is not infallible and comparing both the discordance is notorious, not slight but very notorious.
Your link, by the origin of the agency must have used 460TB which is discontinued, and even if they use BT960, results can't be taken as accurate as well. It is needed a third method of test other than 460TB to verify BT960. (460TB is currently out of production).
In the "mechanism" shown above, the method of measure pyrazinamide susceptibility can be taken as an testimony but not as evidence because was not in agreement with the another method of measurement.
You have here a crucial challenge for the given results.
Wow, you have gone from ignoring it to making up a bullshit justification based on the test fro TB they used? Can you explain why they MUST have used 460 TB? And perhaps comment on this paper:
https://www.ncbi.nlm.nih.gov/pubmed/16329561
and explain what the words:
BACTEC 460 TB system which has been the "Gold Standard" for automated detection of TB.
Mean? Look, you are not a scientist and so when you try to spout bullshit like this you just look bloody stupid. More to the point, you still haven't responded to the original point, merely tried to undermine it. Unsuccessfully.
Lets continue.
I can barely contain myself.
"Over-expression of rspa"
rspa a glycoprotein which in this case discussing here has the duty of binding to the 30S ribosomal protein S1.
What the mutation does is to "impair" the binding. This is to say, the binding is not strong anymore, it can get loose easily.
Like if you have your teeth binding strongly to your gums, the mutation will cause for you weak setting of the teeth in your mouth. They can fell out after eating an apple.
You do realise just how silly this conflation of a chemical term and a folk term looks. No, of course you don't. Here's one example: what would happen if the binding of oxygen in haemoglobin was strong? you'd asphyxiate as the oxygen would never get released. Whether a strong or weak binding is positive or negative is relative to what it's doing - it's not a degradation, it's just different.
Is it "favorable" for bacteria having weak bonding in its structure?
That depends entirely on the environment and what the bonding is doing.
What the hell is that "over-expression?"
Simply, the increased frequency of losing the characteristic of bonding.
Nope.
HM said:"loss of Alanine"
Another degeneration like the horse losing functional digits. Another example for this case is, you lose your skin capabilities to protect you from the environment.
Again, it's just different. In both cases it depends on the environment. With the fused foot, horses can run faster for longer. That was clearly and advantage at some point. Probably when it met some fast predators.
That is not "adaptation", that is not evolution", that is not "speciation", losing alenanine (amino acids) is degeneration.
It really isn't, it's just different. Perhaps you want to explore this in context rather than grabbing three words and obsessing about the word loss.
Up to here, losing capabilities and structural damage and bonding is what antibiotics cause in our poor Tuberculosis bacterium.
Even so, for the next treatment using the same antibiotics, our hero, the Toobee bacterium survives it.
Wow!
And again, you somehow know to completely ignore my careful explanation of what is going on. That's the smoking gun. the thing you can't bear to engage with. You do, dimly realise the problem with your account, because natural selection is so simple even someone with no education in the area and in terrible denial can see the truth of it, so you ignore it over and over again, while holding on to the simplistic idea that loss of anything means degeneration. You must really struggle with the degeneration of people losing weight, or the degeneration of having a cancer removed and so on.
YOu are giving away your awareness of the problem by ignoring the same ideas over and over again - and indeed ignoring me pointing this out over and over again.
You called it "resistant", the whole evolutionists called it "resistant".
That's right.
However, for our Toobee bacterium, having a deformed body won't make it "resistant" to a new attack.
Think.
Think, because your link is not giving the answer.
Yes it is, very simply. Just like the people without the CCR5, the lack of something stops the infection or the poisoning from doing its damage. As a result, the person or bacteria survives and survives to breed, passing on this variation to the next generation.
Sub said:That mutation either left it better fitted for the environment or it didn't. If it didn't it would tend to die, if it did it would tend to survive. if it died, the unhelpful (in that environment) mutation is lost, if it survived then that helpful (in that environment) mutation would be preserved and contribute to the general fitness (in that environment) of its offspring that carried that mutation. That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
HM said:But, the bacteria have lost characteristics, there is no "accumulation" but lost of characteristics.
The lack of, for example, CCR5, is a characteristic. It's one among many millions. All of the time, reproduction, mutation, transcription errors and so on increase the variation, the number of different characteristics - that's a load of processes increasing the number of characteristics all the time. Meanwhile natural selection eliminates the least successful and accumulates the most successful as those with these characteristics survive to breed.
Show me the "accumulations".
I just did. You'll ignore it, again, becuae you dimly see where youa re wrong but can't bring yourself to admit it.
=EBI have reviewed above each one of the points given in the assumed explanation of the mechanism, and the only thing you can read is the something similar to the following:
Really? you can't have been paying much attention then.
The huge truck hit on the small car caused the car's front lights smashed, the front ball joints went loose, the alignment disturbed and siding to the left, air condition condenser gone, radiator destroyed, engine pushed inside and under the car bumper falling out, and broken windshield on the passenger side due to passenger didn't use seat belt.
Bu that's nothing like what I described. What I described is a massive community of people driving cars. Each one customises their car so every car is lightly different. Some, for example, fit wet weather tyres, some fit jacked up suspension and some strip out the extra weight to improve acceleration.
Then depending on the environment each of these variations confers different advantages. If the area has flooding then the jacked up suspension will allow some cars to drive through puddles while the others get flooded and are scrapped. If racing becomes popular, then the stripped down cars will do better and the jacked up cars will be scrapped. All the time people are trying new customisations and the conditions are always changing. As a result, there will be a tendency for the succesful variations to carry on, buit these too will be modified so there is always more variation to be tested.
That's what I was saying.
HM said:You are telling me that with these conditions, the car is now more "resistant" for the next hit by truck, who's driver is obfuscated to hit again in order to kill the driver of the car because he is his wife's love affair.
Where are the "accumulation of favorable steps"?
No, I'm telling you that once again this is a silly straw man that doesn't remotely represent what I said. Again.
You are an evolutionist and now it happens that you yourself don't understand what he said.
So you keep saying.
Read again your phrase.
That's what Darwin meant by accumulation and why it tends to be positive mutations that accumulate.
"Positive"? HIV positive is something "favorable"... sure... right...
And again, you are deliberately equivocating on the word positive. This is simplyu dishonest and inexcusable. The word positive in HIV positive just means that you have HIV, Positive in the sense of mutation just means that the mutation helps you survive in a particular environment.
____________________________________________________________________
Here is your test of fire. This is an analogy.
Why should I bother, you literally ignored my response to the last challenge. I wonder why that was. Well I don't I think it's because you know you are wrong but think if you keep pushing you'll somehow justify yourself. You will not.
Respond to the analogy applying the discussion topic, replacing the Tuberculosis bacterium by a dude.
If you can't explain it, it is possible because you can't understand evolution and less what I am explaining you several times by now.
Just get on with it.Show me with this analogy.
The bacteria is a guy, 6 feet tall, 180 lbs. regular dude, healthy, good IQ, hard worker man, etc. He will be under attack with chemicals. The mission is to kill him.
Use the method you want, could be dropping chemicals over him from a helicopter, giving him the chemicals in his food, you are free to choose the way to kill the guy in the example.
Show later, after the first attack, he will be attacked again with the same chemicals, but at this time he won't be affected, of if he does, will be very minimum.
Hang on. You are talking about a single guy who dies? I'm sorry to break this to you, but after the first attack this single guy will be dead. The end. Your example is fatally flawed as it has only a single person
In the bacteria example, there will be billions of bacteria and only some will die. The survivors will survive to breed the rest will die.
So for a realistic example let's take a million people and expose them to HIV. one percent of these people don't have a CCR5. They tend to survive. The rest do and tend to die. As a result, in the next generation the majority of people will inherit a lack of a CCR5 pathway and will not become infected. That's so simple i know you must understand it. Which is why I suspect you'll ignore it.
Again.
Sub said:Isn't it? it is clearly explained in that article: reactive oxygen and free radicals denature the protein, lipids and nucleic acid. That's a very clear and well understood process.
Apparently you never read the small print words at the bottom of documents, in this case the superfluous conclusion from the consequences of antibiotics in bacteria. Saying "more resistant" is not what is going on.
Really. Can you give me the precise page number or cut and paste this 'fine print' because I think you just made it up. YOu are so desperate you are resorting to simply saying things that are not true. You can't be doing that by accident.
Read my example of people with bold immune cells, they are not "resistant" but simply "no affected" by the AIDS virus, solely because their defect. They catch a cold, they can suffer liver diseases, stomach problem because other bacteria and viruses won't use immune cells hair as their way to move easily inside the body. Is it a weird case. It is not any "evolutionary step" but a birth defect.
If you want to call something a defect when it stops you from getting HIV then you are going to have to explain the negative effects. What is the precise downside of not having a CCR5 pathway? The upside is clear you don't get HIV. The downsides you describe are simply fantasy. YOu made them up.
Surely you don't know why, and for this reason you still are defending a good for nothing theory.
It's a theory that comfortably explains everything above and one that I think you dimly grasp because you couldn't cherry pick as effectively if you didn't. Why are you so scared of evolution that you will deny the evidence in front of you? If it's not religion (but I still think it is) then why are you so against this theory in particular?
HM said:Because evolution is a scientific religion.
I explained why that made no sense las time. However, you know you are wrong. you wouldn't be able to cherrypick so effectively if you didn't grasp what undermines your account and your increasing reliance on fallacies and fantasies demonstrates your desperation.
Don't forget to answer the analogy.
I did, he died. the end.
Answering properly the analogy from above is the best way to check how well you understand evolution. It is just changing the bacterium for a dude. From here, introduce a treatment with drugs to kill the dude. Show the effects. show that when the dude survives will be "more resistant" to the next attack.
You are quite right. I can only assume that you mean me to work out who the dude is. Let me see, who is a the dude that some people think can die and then come back to life... Who could it be? dies and then comes back to life so you can perform the test a second time. It's Jesus isn't it. So Jesus, isn't killed because of whatever bollocks it is Christians believe about Jesus returning from the dead, presumably as a zombie. So this confers a selective advantage over other humans because he's indestructible. So when he fucks Mary Magdalene and produces a line of little Jesi, psion, I believe they are clled, is this a characteristic that can be passed on? I don't know, finally there's an area you can talk about with authority.
is eternal life transmissible genetically?
Now I've finished taking the piss out of your daft demonstration, I just have to point out that a single example doesn't introduce variation. A billion people? I've answered already.
Best wishes.
Thanks.
HM -
I think it is odd that a discussion begun on how consciousness forms and what it is has developed into a long running rant filled with misinformation and misunderstanding to somehow "disprove" evolution while only relying on this same misinformation and fundamental misunderstanding iof what the fact of evolution can explain, hence there being a bunch of workable theories revolving around evolution.
Small changes over time that either increase or decrease the likelihood of fertility leading to a next generation, and thus continued survival is so not as difficult or as unbelievable as some apparently are thinking.
I find it rather disturbing for the amount of individuals who seem to spend a great chunk of time and effort on illogically and/or in some defiance of reality also continuously working around facts instead of with them just to try and deny their existence in the first place, when all is said and done. Because if any who are arguing against the occurrence of evolution actually had evidence to refute it, then they wouldn't be posting it on an internet forum like this. They'd be submitting their data, findings, and the conclusions drawn from them to everyone to be analyzed in a well-thought-out, properly measured and explained new theory.
Alas, it all reads like bunk. But I suppose I can't expect an individual who warps reality to such an extent to then focus on it.
I'd suggest further study, but it seems you're only going to go at it already illogically biased and with a seeming lack of intent to understand it.
With that said, could we go back to discussing consciousness, how it forms and how to analyze it? Seeing as the whole thread started out relating to that, and all.
Just sayin'.
•AL Amyloidosis
A rare disease caused when an abnormal protein, amyloid, enters tissues or organs
•Chronic B-cell Leukemias
A type of cancer which affects white blood cells
•Chloracne (or similar acneform disease)
A skin condition that occurs soon after exposure to chemicals and looks like common forms of acne seen in teenagers. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides.
•Diabetes Mellitus Type 2
A disease characterized by high blood sugar levels resulting from the body’s inability to respond properly to the hormone insulin
•Hodgkin's Disease
A malignant lymphoma (cancer) characterized by progressive enlargement of the lymph nodes, liver, and spleen, and by progressive anemia
•Ischemic Heart Disease
A disease characterized by a reduced supply of blood to the heart, that leads to chest pain
•Multiple Myeloma
A cancer of plasma cells, a type of white blood cell in bone marrow
•Non-Hodgkin's Lymphoma
A group of cancers that affect the lymph glands and other lymphatic tissue
•Parkinson's Disease
A progressive disorder of the nervous system that affects muscle movement
•Peripheral Neuropathy, Early-Onset
A nervous system condition that causes numbness, tingling, and motor weakness. Under VA's rating regulations, it must be at least 10 percent disabling within one year of herbicide exposure.
•Porphyria Cutanea Tarda
A disorder characterized by liver dysfunction and by thinning and blistering of the skin in sun-exposed areas. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides.
•Prostate Cancer
Cancer of the prostate; one of the most common cancers among men
•Respiratory Cancers (includes lung cancer)
Cancers of the lung, larynx, trachea, and bronchus
•Soft Tissue Sarcomas (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma)
A group of different types of cancers in body tissues such as muscle, fat, blood and lymph vessels, and connective tissues
HM said:There is no doubt that the words "no affected anymore" is not synonymous of "resistant".
"Resistant" is a word that implies the individual will do an effort to hold hard an attack, to hold hard in order to avoid temptation, etc.
In the case of religious people, "resistant" will be to change their thoughts in order of not committing a sin. Resistant by no means is attacking back, it's just a defending action, like a shield.
Same way wolfs and other animals can't control the change in the color of their skin to white color in Winter season, same as well no species have control to make any change in their physical bodies to resist an attack. Just to hide somewhere or cover themselves with no physical power to change their bodies by themselves.
I practically "translated" the whole technical terms in the discussion about bacteria and antibiotics, because I wanted the readers to understand what those terms mean, what the process mean in clear layman language.
When this was done, the result was obvious, the whole technical terms were references of mutations, harmful effects in bacteria. The process bacteria suffered is without question a degenerate process. No one of the effects said bacteria "acquired" or "accumulated" favorable characteristics. On the contrary, deformities and lost of characteristics was the final result.
People who blindingly follow a theory won't be aware of the ridiculous position they are defending with such a fanaticism.
There is no place for being "more resistant" which is an expression used by evolutionists to keep their fantasy alive.
How can people be conscious about reality when fanatics are spreading out fake theories replacing our knowledge in science?
Science is the ruler, theories are just attempts to explain a process.
Same as well after a chemical attack, survivors have children with lots of defects, same as well bacteria which survive will procreate new bacteria with defects, not so new bacteria which is "more resistant".
Just review what are the harmful effects of chemicals in troops which were in contact with agent orange.
https://www.publichealth.va.gov/exposures/agentorange/conditions/index.asp
•AL Amyloidosis
A rare disease caused when an abnormal protein, amyloid, enters tissues or organs
•Chronic B-cell Leukemias
A type of cancer which affects white blood cells
•Chloracne (or similar acneform disease)
A skin condition that occurs soon after exposure to chemicals and looks like common forms of acne seen in teenagers. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides.
•Diabetes Mellitus Type 2
A disease characterized by high blood sugar levels resulting from the body’s inability to respond properly to the hormone insulin
•Hodgkin's Disease
A malignant lymphoma (cancer) characterized by progressive enlargement of the lymph nodes, liver, and spleen, and by progressive anemia
•Ischemic Heart Disease
A disease characterized by a reduced supply of blood to the heart, that leads to chest pain
•Multiple Myeloma
A cancer of plasma cells, a type of white blood cell in bone marrow
•Non-Hodgkin's Lymphoma
A group of cancers that affect the lymph glands and other lymphatic tissue
•Parkinson's Disease
A progressive disorder of the nervous system that affects muscle movement
•Peripheral Neuropathy, Early-Onset
A nervous system condition that causes numbness, tingling, and motor weakness. Under VA's rating regulations, it must be at least 10 percent disabling within one year of herbicide exposure.
•Porphyria Cutanea Tarda
A disorder characterized by liver dysfunction and by thinning and blistering of the skin in sun-exposed areas. Under VA's rating regulations, it must be at least 10 percent disabling within one year of exposure to herbicides.
•Prostate Cancer
Cancer of the prostate; one of the most common cancers among men
•Respiratory Cancers (includes lung cancer)
Cancers of the lung, larynx, trachea, and bronchus
•Soft Tissue Sarcomas (other than osteosarcoma, chondrosarcoma, Kaposi's sarcoma, or mesothelioma)
A group of different types of cancers in body tissues such as muscle, fat, blood and lymph vessels, and connective tissues
Just go to some websites showing that until today children are born with horrible birth defects in Vietnam.
Any one of them shows that victims who are descendants of survivors of the agent orange became more "resistant" to something?
The description is never "resistant" but birth defect, abnormalities, diseases, and more.
Clearly, evolutionists with their obstinate tendency to believe in a different religion -a known scientific religion as evolution-, solely with the objective of denying the biblical narration, they have lost consciousness about reality.
This was my point from the very beginning -you'll see it if you review the whole discussion about evolution in this topic- and still is my point now and always will bemy point, because it has strong and accurate foundation which is corroborate from all point of analysis that the only process in life is degeneration.
I based my position with facts, not so with theories.
Our consciousness is 100% related to what we perceive, to what we experience, to what we learn.
If you grow up receiving erroneous information, your awareness is already challenged and subjected to failure rather than following reality.
I think, people reject truth because fantasy offers hope, happiness, it is great losing control in the mind and leave imagination to rule the brains. Theories of science are competing with religion, when they want to offer a similar hope of "a better future" for humankind.
Reality is that the universe started to die the same moment started into existence. And we will continue the same fate, and no imaginary moving to other planets or bodies with favorable changes will happen, degeneration will take it all.
And you better be conscious that such is our destiny, our human destiny.
So now you're claiming he universe is going to acquire the ability to whimper through some degenerate vacuum mutation?
Is your claim that the current vacuum is a false vacuum, and not the lowest possible energy state?
That sucks. Perhaps if we all pray together, then someone will be able to use the vacuum on our bank accounts? They might get a lint ball from mine.So now you're claiming he universe is going to acquire the ability to whimper through some degenerate vacuum mutation?
Is your claim that the current vacuum is a false vacuum, and not the lowest possible energy state?
Our vacuum cleaner broke the other day, it’s yet another degeneration. I was hoping it would evolve to be resistant to breaking, but nothing has happened yet. I probably didn’t pray hard enough...
That sucks. Perhaps if we all pray together, then someone will be able to use the vacuum on our bank accounts? They might get a lint ball from mine.So now you're claiming he universe is going to acquire the ability to whimper through some degenerate vacuum mutation?
Is your claim that the current vacuum is a false vacuum, and not the lowest possible energy state?
Our vacuum cleaner broke the other day, it’s yet another degeneration. I was hoping it would evolve to be resistant to breaking, but nothing has happened yet. I probably didn’t pray hard enough...
So now you're claiming he universe is going to acquire the ability to whimper through some degenerate vacuum mutation?
Is your claim that the current vacuum is a false vacuum, and not the lowest possible energy state?
One form of human resistance to fire, for example, is protective gear. Another form is not lighting a match while standing in a pool of gasoline in an enclosed space. Both are due to some beneficial mutations that allowed behavior pattern mutations to occur in the imagination of the species before being applied to RL.
Ether, the medium forming space must be decaying same as particles do.
That sucks.Our vacuum cleaner broke the other day, it’s yet another degeneration. I was hoping it would evolve to be resistant to breaking, but nothing has happened yet. I probably didn’t pray hard enough...